Venous valves are found within native venous vessels and are used to assist in returning blood back to the heart in an antegrade direction from all parts of the body. The venous system of the leg for example includes the deep venous system and the superficial venous system, both of which are provided with venous valves that are intended to direct blood toward the heart and prevent backflow or retrograde flow, which can lead to blood pooling or stasis in the leg. Incompetent valves can also lead to reflux of blood from the deep venous system to the superficial venous system and the formation of varicose veins. Superficial veins, which include the greater and lesser saphenous veins, have perforating branches in the femoral and popliteal regions of the leg that direct blood flow toward the deep venous system and generally have a venous valve located near the junction with the deep system. Deep veins of the leg include the anterior and posterior tibial veins, popliteal veins, femoral veins, and iliac veins. Deep veins are surrounded in part by musculature tissue that assists in generating flow due to muscle contraction during normal walking or exercising. Veins in the lower leg have a static pressure while standing of approximately 80-90 mm Hg that may reduce during exercise to 60-70 mm Hg. Despite exposure to such pressures, the valves of the leg are very flexible and can close with a pressure drop of less than one mm Hg.
FIGS. 1A-1B are schematic representations of blood flow through a healthy native valve 104 within a vein 100. Venous valve 104 controls blood flow through lumen 102 of vein 100 via leaflets 106, 108. More particularly, venous valve 104 opens to allow antegrade flow 112 through leaflets 106, 108 as shown in FIG. 1A. Venous valve 104 closes to prevent backflow or retrograde flow 114 through leaflets 106, 108 as shown in FIG. 1B.
Veins typically in the leg can become distended from prolonged exposure to excessive pressure and due to weaknesses found in the vessel wall causing the natural venous valves to become incompetent leading to retrograde blood flow in the veins. Such veins no longer function to help pump or direct the blood back to the heart during normal walking or use of the leg muscles. As a result, blood tends to pool in the lower leg and can lead to leg swelling and the formation of deep venous thrombosis and phlebitis. The formation of thrombus in the veins can further impair venous valvular function by causing valvular adherence to the venous wall with possible irreversible loss of venous function. Continued exposure of the venous system to blood pooling and swelling of the surrounding tissue can lead to postphlebitic syndrome with a propensity for open sores, infection, and may lead to possible limb amputation.
Chronic Venous Insufficiency (CVI) occurs in patients that have deep and superficial venous valves of their lower extremities (below their pelvis) that have failed or become incompetent due to congenital valvular abnormalities and/or pathophysiologic disease of their vasculature. As a result, these patients suffer from varicose veins, swelling and pain of the lower extremities, edema, hyper pigmentation, lipodermatosclerosis, and deep vein thrombosis (DVT). Such patients are at increased risk for development of soft tissue necrosis, ulcerations, pulmonary embolism, stroke, heart attack, and amputations.
FIG. 2 is a schematic representation of blood flow through an incompetent venous valve. Backflow or retrograde flow 114 leaks through venous valve 104 creating blood build-up that eventually may destroy the venous valve and cause a venous wall bulge 110. More specifically, the vessel wall of vein 100 expands into a pouch or bulge, such that the vessel has a knotted appearance when the pouch is filled with blood. The distended vessel wall area may occur on the outflow side of the valve above leaflets 106, 108 as shown in FIG. 2, and/or on the inflow side of the valve below leaflets 106, 108. After a vein segment becomes incompetent, the vessel wall dilates and fluid velocity there through decreases, which may lead to flow stasis and thrombus formation in the proximity of the venous valve.
Repair and replacement of venous valves presents a formidable problem due to the low blood flow rate found in native veins, the very thin wall structure of the venous wall and the venous valve, and the ease and frequency of which venous blood flow can be impeded or totally blocked for a period of time. Surgical reconstruction techniques used to address venous valve incompetence include venous valve bypass using a segment of vein with a competent valve, venous transposition to bypass venous blood flow through a neighboring competent valve, and valvuloplasty to repair the valve cusps. These surgical approaches may involve placement of synthetic, allograft and/or xenograft prostheses inside of or around the vein. However, such prostheses have not been devoid of problems leading to thrombus and/or valve failure due to leaflet thickening/stiffening, non-physiologic flow conditions, non-biocompatible materials and/or excessive dilation of the vessels with a subsequent decrease in blood flow rates.
The aortic valve is located at the intersection of the left ventricle of the heart and the ascending aorta. During ventricular systole, pressure rises in the left ventricle. When the pressure in the left ventricle rises above the pressure in the aorta, the aortic valve opens, allowing blood to exit the left ventricle into the aorta. When ventricular systole ends, pressure in the left ventricle rapidly drops. When the pressure in the left ventricle decreases, the aortic pressure forces the aortic valve to close.
FIGS. 3A-3B are schematic representations of blood flow through a healthy aortic valve 304 at the intersection of aorta 302 and left ventricle 306. Aortic valve 304 controls blood flow from left ventricle 306 to aorta 302. More particularly, aortic valve 304 opens to allow antegrade flow 312 through aortic valve 304 as shown in FIG. 3A. Aortic valve 304 closes to prevent backflow or retrograde flow 314 through aortic valve 304 as shown in FIG. 3B.
FIG. 5 is a schematic illustration of the junction between the aorta 302 and the heart. The aortic root 318 is the portion of the left ventricular outflow tract which supports the leaflets 334 (shown in FIG. 6) of the aortic valve 304. The aortic root 318 may be delineated by the sinotubular junction 336 distally and the bases of the valve leaflets 334 proximally. The aortic root 318 comprises the sinuses 332, the valve leaflets 334, the commissures 340, and the interleaflet triangles (not shown). The annulus 338 is the area of collagenous condensation at the point of leaflet attachment. The annulus 338 comprises a dense fibrous ring attached either directly or indirectly to the atrial or ventricular muscle fibers.
Aortic insufficiency (AI), also called aortic regurgitation, occurs when the aortic valve does not close completely when pressure in the left ventricle drops at the end of ventricular systole. Such a failure to close causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle of the heart. This means that some of the blood that was already ejected from the heart is regurgitated back into the heart. The percentage of blood that regurgitates back through the aortic valve due to AI is known as the regurgitant fraction. Since some of the blood that is ejected during systole regurgitates back into the left ventricle during diastole, there is decreased effective forward flow in AI. Aortic insufficiency causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart.
FIG. 4 is a schematic representation of blood flow through an incompetent aortic valve 304. Backflow or antegrade flow 314 leaks through aortic valve 304 such that blood regurgitates back into the left ventricle 306.
Aortic insufficiency can be due to abnormalities of either the aortic valve or the aortic root. The surgical treatment of choice at this time is an aortic valve replacement. This is currently an open-heart procedure, requiring the individual to be placed on cardiopulmonary bypass. Further, any replacement or treatment of the aortic valve must take into account the coronary arteries. The coronary arteries (left and right) (not shown) originate from the aortic root 318 (more particularly the sinuses 332), immediately above the aortic valve. The coronary arteries supply oxygen rich blood to the muscle tissue of the heart (the myocardium). The junction of the coronary arteries with the sinuses is called the coronary ostia. The left coronary ostium 350 and right coronary ostium 352 are shown in FIGS. 9B, 13A, and 13B. The coronary ostia cannot be blocked by the replacement valve.
Similarly, pulmonary valve 310 (shown in FIGS. 3A-3B) controls blood flow from the right ventricle 311 to the main pulmonary artery 308, and eventually to the lungs. More particularly, pulmonary valve 310 opens to allow antegrade flow through pulmonary valve 310. Pulmonary valve 310 closes to prevent backflow or retrograde flow through pulmonary valve 310 back into right ventricle 311. Pulmonary valve insufficiency or regurgitation occurs when the pulmonary valve 310 does not close properly after the right ventricle 311 has finished its pumping cycle. Excess blood therefore makes the right ventricle 311 work harder than normal.
As with aortic valve insufficiency, pulmonary valve insufficiency can be due to abnormalities of either the pulmonary valve or the annulus. The surgical treatment of choice at this time is a pulmonary valve replacement. This is currently an open-heart procedure, requiring the individual to be placed on cardiopulmonary bypass.
Throughout this specification, references to a heart valve, aortic valve, or pulmonary valve can apply equally to both the aortic valve and the pulmonary valve, except where specifically noted. Thus, structures described below for the aortic valve apply equally to the pulmonary valve.
In view of the foregoing, there is still a need for methods and apparatus to restore normal venous circulation to patients suffering from venous valve insufficiency and normal circulation to the aorta to patients suffering from aortic valve insufficiency, wherein the methods and apparatus may be used in percutaneous, minimally invasive procedures.